1. Field of the Invention
This invention concerns a device positionable in an opening in a flexible membrane or in the lumen of a vessel having a flexible sidewall. The device distends or biases opposite portions defining the opening or forming the vessel sidewall outwardly in the plane of the device. The outward biasing draws opposing portions of the opening or sidewall inwardly in a direction perpendicular to the plane of the device and into apposition or contact.
2. Description of Related Art
Elastic membranes, in particular, living tissue such as muscular tissue, may be subject to defects, disorders or diseases wherein unwanted openings or cavities are formed through or in the tissue. Elastic vessels having flexible sidewalls are found extensively throughout the human body and perform a variety of vital functions, for example, carrying and distributing blood to tissue and transporting waste matter from the digestive and urinary systems. The vessels may use sphincters to control the flow of matter through the vessels or they may incorporate one-way valves to prevent back flow of fluid. The valves and even the vessels themselves may suffer from defects, disorders or abnormalities which inhibit their ability to function properly. Examples of various disorders of important muscular tissue as well as blood vessels are described below by way of specific examples.
Mitral Valve Incompetence
As shown in FIG. 1, the left atrioventricular or mitral valve 2 is a bicuspid (two-leaflet) valve positioned in the orifice 4 between the left atrium 6 and left ventricle 8 of the heart 10. Oxygen rich blood 12 flows from the lungs via pulmonary veins 14 to the left atrium 6, past the mitral valve 2 and into the left ventricle 8 where it is pumped to the aorta 16 for further distribution to the body. The mitral valve 2 has leaflets 18 and 20 in apposition to one another defining the plane 22 of the valve parallel to and between the leaflets. The mitral valve 2 is a one way valve, its leaflets 18 and 20 moving perpendicularly to the valve plane 22 away from one another to permit flow into the left ventricle 8, and closing against one another (also known as coaptation) in response to a pressure increase in the left ventricle 8 caused when it contracts to pump the blood through the aorta 16. In a healthy valve, the leaflets 18 and 20 normally seal against each other (coapt) to prevent back flow of blood through the left atrium 6 to the lungs. However, in a diseased mitral valve the leaflets may prolapse into the left atrium and allow a back flow of blood.
Of the various valves in the heart, the mitral valve is most vulnerable to disease and suffers from atrioventricular valvular incompetence whereby the mitral valve seals incompletely. This allows blood to regurgitate into the left atrium upon contraction of the left ventricle. The diseased leaflets of the valve undergo scarring and shortening which are one cause the valvular incompetence. Other causes include abnormal elongation of the chordae tendineae (tendinous cords attached to the free edges of the leaflets to prevent prolapse), as well as rigidity, deformity and retraction of the leaflets associated with rheumatic heart disease.
Due to the low success rate associated with mitral valve replacement, atrioventricular valvular incompetence is preferably treated by mitral valve repair requiring open heart surgery. This treatment is extremely invasive, requires that the heart be stopped and the patient put on cardiopulmonary bypass and often leads to post-operative complications.
Venous Valve Incompetence
As shown in FIG. 2, the veins 24 of the human circulatory system have a system of one-way valves such as 26 and 28, also comprising two leaflets 30 and 32, which operate to promote the flow of blood from the extremities back to the heart by preventing the retrograde flow of blood to the extremities between heart beats. The venous valves 26 and 28 also cooperate to allow muscular action to assist in the pumping of blood from the venous side of the circulatory system back to the heart. The contraction of various muscles 34 tends to constrict the veins 24, forcing blood to flow out of the vein, and the venous valves 26 and 28 cooperate, with valve 28 opening while valve 26 remains closed, to permit only one-way flow back to the heart.
The veins are subject to various disorders related to defective structure and function of their valves, known as valve incompetence. Valve incompetence can cause varicose veins, as well as chronic venous insufficiency wherein the valve leaflets become thickened and contracted so that they become incapable of preventing the retrograde flow of blood. Both of these conditions cause considerable discomfort and can lead to further complications such as edema, erythema, dermatitis, skin ulceration and cellulitis.
Arterial Saccular Aneurysms
As illustrated in FIG. 3, saccular aneurysms 36 occur at the branching 38 of arteries 40 in the body and comprise a sack-like formation of the artery wall 42 which extends outwardly from the bifurcation point 44 between the arterial branches 40. The aneurysm 36 has a neck 46 of reduced diameter forming the juncture with the artery 40 and is capped by a dome 48. During formation of the aneurysm 36, the arterial internal elastic lamina disappears at the neck 46, the wall 42 thins and weakens and connective tissue replaces smooth-muscle cells. The aneurysm tends to rupture at the dome 48 and bleeding ensues.
Rupture of a cerebrovascular saccular aneurysm is especially serious due to the associated high mortality rate (10% within the first day of rupture, 25% within three months) and the major neurological deficits experienced by those who survive the initial hemorrhage.
Patent Foramen Ovale
As shown in FIG. 1, the foramen 3 is an opening in the muscle tissue of the heart between the left and right atria (6 and 7 respectively). This opening is present before birth to allow blood to be channeled between the mother and the fetus. After birth the foramen normally closes to separate the atria and allow blood to be pumped by the infant's heart. Patent foramen ovale is a heart defect wherein the foramen fails to close after birth and allows leakage of blood between the atria. This defect results in a greater risk of pulmonary embolism and stroke.
Atrial Appendage
FIG. 1B is a partial sectional view taken at line 1B—1B in FIG. 1 and illustrates an atrial appendage 5 extending from the left atrium 6 adjacent to the pulmonary trunk 9. The atrial appendage 5 is approximately the size of a human thumb and performs no known useful function. It is, however, responsible for the formation of blood clots, and is believed to be responsible for 90 percent of strokes associated with non-rheumatic atrial fibrillation, or irregular heart beat. The risk of stroke is greatly reduced by closing off the atrial appendage 5 from the left atrium 6.
Atrial and Ventricular Septal Defects
An atrial septal defect, illustrated in FIG. 1C, is a heart defect characterized by an opening 13 in the septum or wall 15 separating the left and right atria 6 and 7 respectively. Similarly, a ventricular septal defect is characterized by an opening 17 in the septum 19 separating the left and right ventricles 8 and 11 respectively. Such openings allow blood to flow between the atria or the ventricles.
If untreated, an atrial septal defect places stress on the right ventricle which may dilate and weaken in response. The lungs may become congested and pulmonary hypertension may also result, as well as arrhythmias and blood clots leading to stroke. A ventricular septal defect also places greater stress on the right ventricle, again leading to congestion, pulmonary hypertension, blood clots, stroke and arrhythmia.
There is a need, therefore, for a device and a method which can be used to correct disorders and abnormalities associated with opening in muscular tissue as well as vessels having flexible, elastic sidewalls and which may be employed in a safe, minimally invasive manner to reduce trauma to the patient and minimize post-operative complications.